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T Cell Activation and Clonal Selection

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...

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Visualizing Cell-to-cell Transfer of HIV using Fluorescent Clones of HIV and Live Confocal Microscopy

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HIV Expression in Infected T Cell Clones.

Jason W Rausch¹, Shadab Parvez¹, Sachi Pathak¹

¹HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA.

|January 23, 2024

Summary

The persistence of HIV-1 infected cells, driven by viral latency and T cell proliferation, is a major hurdle to a cure. Understanding these factors is key to developing strategies for HIV-1 eradication.

Keywords:

HIV rebound T cell clonal expansion human immunodeficiency virus (HIV)persistence transcriptional regulation

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Area of Science:

Immunology
Virology
Cell Biology

Background:

Antiretroviral therapy (ART) suppresses HIV-1 replication but does not eliminate the virus.
The primary barrier to an HIV-1 cure is the persistence of infected cells harboring replication-competent proviruses.
Viral latency and cellular proliferation are key determinants of HIV-1 persistence.

Purpose of the Study:

To review the genetic, epigenetic, cellular, and immunological factors influencing HIV-1 transcriptional suppression.
To discuss the clonal expansion of HIV-1 reservoir T cells.
To explore the interdependencies among these determinants and their implications for HIV-1 persistence.

Main Methods:

This review synthesizes existing research on HIV-1 persistence.
It examines the mechanisms of viral latency and cellular proliferation in CD4+ T cells.
The review discusses the interplay between genetic, epigenetic, cellular, and immunological factors.

Main Results:

HIV-1 transcriptional suppression (latency) allows infected cells to evade immune detection.
CD4+ T cell proliferation can facilitate HIV-1 propagation without detrimental viral gene expression.
Selective pressures on ART favor the expansion of latently infected cell clones.

Conclusions:

Incomplete or reversed latency in expanding clones can lead to persistent low-level viremia and rebound after treatment cessation.
Understanding the determinants of viral latency and clonal expansion is crucial for developing strategies to eliminate the HIV-1 reservoir.
Targeting these persistence mechanisms may offer new avenues for achieving a functional HIV-1 cure.